Horn E M, Waldrop T G
Department of Physiology and Biophysics, University of Illinois, Urbana 61801.
Brain Res. 1994 Nov 21;664(1-2):25-33. doi: 10.1016/0006-8993(94)91949-6.
Prior results from this laboratory have demonstrated that the respiratory response to hypercapnia is enhanced by microinjection of GABA antagonists or GABA synthesis inhibitors into the caudal hypothalamus of both cats and rats. However, no evidence was found for modulation of the respiratory response to hypoxia by a hypothalamic GABAergic mechanism. The purpose of the present study was to determine if synaptic input other than GABAergic onto caudal hypothalamic neurons affects the respiratory responses to hypoxia. The respiratory (diaphragmatic EMG) responses to hypoxia (10% O2) and hypercapnia (5% CO2) were recorded in anesthetized rats before and after bilateral microinjection of a blocker of synaptic transmission (CoCl2, 100 mM) or an excitatory amino acid receptor antagonist (kynurenic acid, 50 mM) into the caudal hypothalamus. Both hypoxia and hypercapnia elicited increases in tidal diaphragmatic activity and respiratory frequency prior to the microinjections. The respiratory response to hypercapnia was increased (+10.5%) after CoCl2 microinjections, which is consistent with prior results obtained with blockade of GABAergic input. Kynurenic acid did not alter the respiratory response to hypercapnia. A new finding was that the respiratory response to hypoxia was diminished after both CoCl2 (-13.0%) and kynurenic acid (-25.0%) microinjections. The results of this study support our prior findings that neurons in the caudal hypothalamus modulate the respiratory response to hypercapnia. In addition, our findings suggest that an excitatory input acting through excitatory amino acid receptors in the caudal hypothalamus modulates the respiratory responses to hypoxia.
该实验室先前的研究结果表明，通过向猫和大鼠的下丘脑尾部微量注射GABA拮抗剂或GABA合成抑制剂，可增强对高碳酸血症的呼吸反应。然而，未发现下丘脑GABA能机制对低氧呼吸反应有调节作用。本研究的目的是确定除GABA能之外，下丘脑尾部神经元的其他突触输入是否会影响对低氧的呼吸反应。在双侧向下丘脑尾部微量注射突触传递阻滞剂（CoCl2，100 mM）或兴奋性氨基酸受体拮抗剂（犬尿氨酸，50 mM）之前和之后，记录麻醉大鼠对低氧（10% O2）和高碳酸血症（5% CO2）的呼吸（膈肌肌电图）反应。在微量注射前，低氧和高碳酸血症均引起膈肌潮气量活动和呼吸频率增加。CoCl2微量注射后，对高碳酸血症的呼吸反应增强（+10.5%），这与先前阻断GABA能输入所获得的结果一致。犬尿氨酸未改变对高碳酸血症的呼吸反应。一个新发现是，CoCl2（-13.0%）和犬尿氨酸（-25.0%）微量注射后，对低氧的呼吸反应均减弱。本研究结果支持我们先前的发现，即下丘脑尾部的神经元调节对高碳酸血症的呼吸反应。此外，我们的研究结果表明，通过下丘脑尾部兴奋性氨基酸受体起作用的兴奋性输入调节对低氧的呼吸反应。
